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[腺苷A1受体和线粒体钾ATP通道在低氧和高碳酸血症联合作用下增强急性低氧耐受性机制中的作用]

[The role of adenosine Al receptors and mitochondrial K+ATP channels in the mechanism of increasing the resistance to acute hypoxia in the combined effects of hypoxia and hypercapnia].

作者信息

Tregub P P, Kulikov V P, Stepanova L A, Zabrodina A S, Nagibaeva M E

出版信息

Patol Fiziol Eksp Ter. 2014 Oct-Dec(4):48-52.

Abstract

We studied the role of the role of mitoK+ATp channels and Al-adenosine receptor in the mechanism of increasing the resistance to acute hypoxia after hypoxic, hypercapnic and hypercapnic-hypoxic preconditioning. It is shown that mitochondrial ATP-sensitive potassium channels and Al-adenosine receptors, an important mechanism of preconditioning have a high value to increase the resistance to acute hypoxia/ischemia in the combined effect of hypoxia and hypercapnia. However, with regard to the adenosine receptor, this mechanism is realized without the participation hypercapnic component, which apparently starts neuroprotection without activation of the adenosine Al receptors.

摘要

我们研究了线粒体钾离子ATP通道和A1-腺苷受体在低氧、高碳酸血症及高碳酸血症-低氧预处理后增强急性低氧耐受性机制中的作用。结果表明,线粒体ATP敏感性钾通道和A1-腺苷受体作为预处理的重要机制,在低氧和高碳酸血症联合作用下,对于增强急性低氧/缺血耐受性具有重要价值。然而,对于腺苷受体而言,该机制是在没有高碳酸血症成分参与的情况下实现的,高碳酸血症成分显然在未激活腺苷A1受体的情况下启动了神经保护作用。

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